Acute renal failure (ARF) презентация

DEFINITION
Acute renal failure (ARF) is an abrupt and sudden reduction in renal function resulting in the inability to excrete metabolic wastes and maintain proper fluid & electrolyte balance

DEFINITION
It is usually associated with oliguria (urine output <30cc/hr or <400cc/day), although urine output may be normal or increased
BUN & creatinine values are elevated

FUNCTIONS OF THE KIDNEY’S
Urine Formation: Formed in the nephrons through a complex three-step process:
Glomerular filtration (GF)
Tubular reabsorption,
Tubular secretion
Excretion of waste products: eliminates the body’s metabolic waste products (urea, creatinine, phosphates, sulfates)

KIDNEY FUNCTIONS
Control of water balance: Normal ingestion of water daily is 1-2L and normally all but 400-500mL is excreted in the urine
Osmolality: degree of dilution or concentration of urine (#particles dissolved/kg urine (glucose & proteins are osmotically active agents)
Specific Gravity: measurement of the kidney’s ability to concentrate urine (weight of particles to the weight of distilled water)
ADH: vasopressin – regulates water excretion and urine concentration in the tubule by varying the amount of water reabsorbed.

FUNCTIONS OF THE KIDNEY’S
Regulation of electrolytes: volume of electrolytes excreted per day is exactly equal to the volume ingested
Na – allows the kidney to regulate the volume of body fluids, dependent on aldosterone (fosters renal reabsorption of Na)
K – kidneys are responsible for excreting more than 90% of total daily intake
RETENTION OF K IS THE MOST LIFE-THREATENING EFFECT OF RENAL FAILURE

FUNCTIONS OF THE KIDNEY’S
Control of blood pressure: BP monitored by the vasa recta.
Juxtaglomerular cells, afferent arteriole, distal tubule, efferent arteriole
Renal clearance: ability to clear solutes from plasma
Dependent on… rate of filtration across the glomerulus, amount reabsorbed in the tubules, amount secreted into the tubules
CREATININE
Regulation of red blood cell production: Erythropoeitin is released in response to decreased oxygen tension in renal blood flow. This stimulates the productions of RBCs (increases amount of hemoglobin available to carry oxygen)

KIDNEY FUNCTIONS
Regulation of acid-base balance: elimination of sulphuric and phosphoric acid

ANATOMY OF THE KIDNEY

NEPHRON

RENIN-ANGIOTENSIN SYSTEM

PATHOPHYSIOLOGY
Glomerular filtration is caused by difference between glomerular pressure (70 mm Hg), colloid oncotic pressure (30 mm Hg) and capsular pressure (20 mm Hg).
The effective filtration pressure is
70mmHg -(30mmHg + 20mmHg) = 20mmHg.
Oncotic + capsular pressure must be lower than glomerular pressure. As a result of the filtration primary urine is formed.

PATHOPHYSIOLOGY
As a result of the filtration primary urine is formed.
The kidneys produce 180 to 200 l of filtrate per day.
This fluid is essentially protein-free and contains mostly crystalloids in the same concentrations as in the plasma.
Approximately 99% of the filtrate must be returned to the vascular system, while 1% is excreted in the urine.

PATHOPHYSIOLOGY
The return flow of filtered molecules from the tubules to the blood is called reabsorption
Tubules reabsorb 179 l of water, 1kg of NaCl, 500g of NaHCO3, 250g of glucose, 100g of amino acids per day
Some substances are not being reabsorbed; such as: urea, uric acid, creatinine etc.
As a result of the reabsorption, secondary urine is formed (1-2 l per day).
Some substances are secreted by tubular cells (bases, acids, drugs, etc.).

EPIDEMIOLOGY OF ARF
Incidence, etiology and outcome varied depending on Population studied and Definition used
Mostly in-Patient than out –Patient
5-7% of hospital admissions
Mortality varies between 20%-85% depending on cause

CLASSIFICATION
ARF may occur in 3 clinical settings:
As an adaptive response to severe volume depletion and hypotension, with structurally and functionally intact nephrons (Prerenal)
In response to cytotoxic or ischemic insults to the kidney, with structural and functional damage (Intrinsic or Intrarenal)
Obstruction to the passage of urine (Postrenal)

CLASSIFICATION
Prerenal
As many as 70% of patients with ARF are prerenal.
Reduced renal perfusion caused by
hypovolemia (volume depletion),
low cardiac output states,
or profound systemic vasodilation (volume redistribution)
.

CLASSIFICATION
Prerenal
Afferent arteriolar vasodilation and efferent vasoconstriction of the glomerular vessels (mediated by dilating prostaglandins and angiotensin II, respectively) will initially maintain glomerular perfusion pressure at a cost of compromising tubular perfusion.
If renal hypoperfusion persists, acute tubular necrosis and established renal failure inevitably develop.

CLASSIFICATION
The causes of prerenal ARF include the following:
volume depletion
gastrointestinal loss,
excessive diuresis,
and salt-wasting nephropathy
volume redistribution (peripheral vasodilation)
peritonitis, burns, pancreatitis,
hypoalbuminemia
reduced cardiac output
pericardial tamponade,
myocardial infarction,
acute/chronic valvular disease,
cardiomyopathies,
arrhythmias.

CLASSIFICATION
Intrinsic
Intrinsic cases comprise 25% of all acute renal failure cases.
Most cases (90%) of acute intrinsic renal failure are
acute tubular necrosis caused by renal ischemia and toxins (including sepsis).
The terminal portion of the proximal tubule and the ascending limb of the loop of Henle are most at risk because of their high metabolic activity.
Epithelial casts develop, blocking the tubules and
further impairing function.
Recovery of function is common following acute
tubular necrosis, and is brought about by renal parenchymal regeneration.

CLASSIFICATION
The causes of intrinsic renal failure include:
renal ischemia
renal artery/vein thrombosis
glomerulonephritis
vasculitides
hemolytic uremic syndrome/thrombotic thrombocytopenic purpura
malignant hypertension
drugs (eg, aminoglycosides, contrast media)
acute tumor lysis syndrome
rhabdomyolysis
allergic interstitial nephritis
acute pyelonephritis.

POST-RENAL ARF
Obstruction – complete or Partial
Anuria or variable urine output
Recovery depends on duration of obstruction
Conditions Sonogram may not show obstruction,
Retroperitoneal fibrosis
Tumors
Adenopathy
Encasing ureter prevent dilatation
Postrenal causes are typically reversible

PHASES OF ACUTE RENAL FAILURE
Clinical progression of reversible RF occurs in four phases:
Initiation phase
Begins with initial insult and ends when oliguria develops
Oliguric phase
Accompanied by rise in serum concentrations of substances usually excreted by kidneys (urea, creatinine, ua, organic acids, intracellular cations [K+ & Mg])
urinary output <400cc/day
May last 1-3 weeks

PHASES OF ACUTE RENAL FAILURE
Diuretic phase
The kidneys begin to recover
Initially produce hypotoniс urine d/t increase in GFR
Recovery phase
Tubular function restored
Diuresis subsides and kidney begins to function normally again

DIAGNOSIS
While a medical history and physical examination are important in making a diagnosis of acute renal failure, laboratory findings help to define the diagnosis.

DIAGNOSIS
History
Observe for disorder that predisposes pt to ARF
Ask questions about recent illness, infections, or injuries
Medication history
Urinary patterns
History of GI problems
Psychosocial
Anxious
Family members

CLINICAL MANIFESTATIONS OF ARF
Cardiovascular
Arrhythmias
BP, N, high or low
Anemia
P, rapid, bounding, or N
Pericardial-type chest pain
Respiratory
Dyspnea
Crackles
Tachypnea
Kussmaul’s respirations
Mental Status
Lethargy
Tremors
Memory loss
Confusion
Musculoskeletal
Muscle spasms
Weakness

CLINICAL MANIFESTATIONS OF ARF
Genitourinary
Oliguria
Anuria
abN urine colour, clarity, smell
GI
Moist tongue & increased saliva
Dry tongue & mucous membranes
N&V
Integumentary
Moist, warm skin & pitting edema
Decreased skin turgor
bruises
Pallor
Thin, brittle hair & nails

DIAGNOSIS
Oliguria (urine output < 400 mL/day) may or may not be present. The important laboratory abnormalities include:
raised urea and creatinine
hyperkalemia
metabolic acidosis.
All of the above problems will be exacerbated if they are caused or accompanied by the hypercatabolic state of the systemic inflammatory response syndrome (SIRS) or sepsis. Urinalysis aids the distinction between prerenal and intrinsic renal failure.
The urinary bladder must be catheterized and appropriate imaging (ultrasound, CT) performed to exclude obstruction of the renal tract.
Autoimmune screens for disorders such as systemic lupus erythematosus (SLE),Wegener’s granulomatosis, and Goodpasture syndrome might be indicated,along with renal biopsy if the cause is uncertain.

The fractional excretion of sodium (FENa+) is considered to be the most reliable biochemical laboratory discriminator between prerenal and intrinsicrenal failure, and is given by:
FENa+ = (UNa/PlNa)/(UCr/PlCr)× 100
where UNa = urea sodium, PlNa = plasma sodium, UCr = urea creatinine, and PlCr = plasma creatinine.
The fractional excretion of urea can also be particularly useful in assessing prerenal cases.

DIAGNOSIS
Distinction between prerenal and intrinsic ARF
ARF , acute renal failure; FE Na+, fractional excretion of Na+.

OLIGURIC PHASE
Hypervolemia
Elevated blood urea nitrogen and serum creatinine levels
Normal or decreased serum sodium level
Hyperkalemia
Metabolic acidosis

TREATMENT
Prerenal renal failure
The aim of treatment is to restore renal perfusion before intrinsic renal failure is established.
Recent ‘renal rescue’ protocols emphasize the need for:
invasive monitoring
aggressive fluid resuscitation
restoration of the patient’s systolic blood pressure to a normal level
avoidance of nephrotoxins
maintenance of adequate oxygenation, with artificial ventilation if necessary

TREATMENT
Intrinsic renal failure
Renal perfusion should be maintained to eliminate prerenal failure.
Measures should be taken to exclude and treat obstructive renal failure.
Once intrinsic renal failure is established, general measures can be adopted and these are discussed below.
Fluid balance
Restrict fluid intake to 30 mL/h plus losses (nasogastric, drains, diarrhea, etc) until renal replacement therapy has been instituted.

TREATMENT
Nutritional support
Adequate nutrition is of considerable importance and should be enteral if at all possible.
Caloric requirements may be high in hypercatabolic patients (30–35 kcal/kg daily).
Protein intake should be restricted to 20–30 g daily

TREATMENT
Treatment of hyperkalemia
Treatment is required if EKG changes are present or potassium (K+) levels >6.5 mmol/L.
EKG changes signaling hyperkalemia include:
• peaked T waves
• loss of P wave
• broadened QRS complex
• slurring of ST segment into T wave
• sine wave leading to asystole.

TREATMENT
If dialysis is not immediately available, the following measures may be used to temporarily redistribute K+ from the plasma or stabilize the myocardium to reduce the risk of arrhythmias:
• Calcium gluconate (10%) 10 mL i.v. over 5 min (or 20 mL if there is hypocalcemia) will reduce the risk of arrhythmias.
• Glucose (50%) 50 mL i.v. will stimulate insulin release, thereby promoting entry of K+ (and glucose) into cells. If hyperglycemia ensues, administer 4–12 units of insulin (routine use of insulin in patients who do not have diabetes carries an unnecessary risk of hypoglycemia).

TREATMENT
• If the patient is acidotic, give sodium bicarbonate (NaHCO3) 50–100 mmol over 1 h but be aware of the usual risks of bicarbonate administration, including fluid overload, worsening of intracellular and cerebrospinal fluid (CSF) acidosis, acute ionized hypocalcemia, and increased carbon dioxide production.
• Eliminate any unnecessary K+ administration in drugs, diet, etc.

TREATMENT
Treatment of acidosis
Sodium bicarbonate should be used only when acidosis is severe (pH <7.1), the patient is symptomatic, or if acidosis is associated with acute hyperkalemia.
The need for bicarbonate is an indication for dialysis.

TREATMENT
Identification and treatment of sepsis
Commence empiric broad-spectrum therapy once cultures have been taken, bearing in mind the potential nephrotoxicity and reduced elimination of many antimicrobials.

TREATMENT
Cause-specific therapies :
• mannitol/NaHCO3 in acute rhabdomyolysis
• immunosuppression in SLE, Wegener’s granulomatosis, or Goodpasture syndrome
• plasmapheresis, fresh frozen plasma, and prostacyclin in the hemolytic uremic syndrome
• steroids in allergic interstitial nephritis.

HEMODIALYSIS
Who needs dialysis? Guidelines for the initiation of renal replacement therapy
Severe hyperkalaemia, unresponsive to medical therapy
Fluid overload with pulmonary oedema (in the context of acute renal failure)
Uraemia (blood urea >30–50 mmol/l)
Complications of severe uraemia: encephalopathy, pericarditis, neuropathy/myopathy
Severe acidosis (pH <7.1)
Drug overdose with a dialysable toxin

HEMODIALYSIS
Dialysis is a type of renal replacement therapy which is used to provide artificial replacement for lost kidney function due to acute or chronic kidney failure
It is a life support treatment, it does not cure acute or chronic renal failure
May be used for very sick clients who have suddenly lost kidney function
May be used for stable clients who have permanently lost kidney function

HEMODIALYSIS
Healthy kidneys remove waste products (potassium, acid, urea) from the blood and they also remove excess fluid in the form of urine
Dialysis has to duplicate both of these functions
Dialysis – waste removal
Ultrafiltration – fluid removal

PRINCIPLE OF DIALYSIS
Dialysis works on the principle of diffusion of solutes along a concentration gradient across a semipermiable membrane
Blood passes on one side of the semipermeable membrane, and a dialysis fluid is passed on the other side
By altering the composition of the dialysis fluid, the concentrations of the undesired solutes (potassium, urea) in the fluid are low, but the desired solutes (sodium) are at their natural concentration found in healthy blood

HEMODIALYSIS
Client’s blood is passed through a system of tubing (dialysis circuit) via a machine to a semipermeable membrane (dialyzer) which has the dialysis fluid running on the other side
The cleansed blood is then returned via the circuit back to the body
The dialysis process is very efficient (much higher than in the natural kidneys), which allows treatments to take place intermittently (usually 3 times a week), but fairly large volumes of fluid must be removed in a single treatment which can be very demanding on a client

ACUTE RENAL SUPPORT
is usually performed as 4-h sessions daily
or on alternate days.
It is highly effective, correcting biochemical, metabolic,
and acid–base derangements,
but it can be impossible to remove sufficient fluid
without provoking severe hypotension that might require cardiovascular support.
Risks of dysequilibrium and cerebral edema are highest with this method.
Intermittent hemodialysis

EQUIPMENT NEEDED FOR HD
The HD machine performs the function of pumping the patient's blood and the dialysate through the dialyzer.
The newest dialysis machines on the market are highly computerized and continuously monitor an array of safety-critical parameters, including blood and dialysate flow rates, blood pressure, heart rate, conductivity, pH, etc.
If any reading is out of normal range, an audible alarm will sound to alert the patient-care technician who is monitoring the patient.

HEMODIALYSIS

The side effects
are proportionate to the amount of fluid being removed
Decreased blood pressure
Fatigue
Chest pains
Leg cramps
Headaches
Electrolyte imbalance
N&V
Reaction to the dialyzer
Air embolism

Complications of HD
Because HD requires access to the circulatory system, clients have a portal of entry for microbes, which could lead to infection
The risk of infection depends on the type of access used
Bleeding may also occur at the access site
Blood clotting was a serious problem in the past, but the incidence of this has decreased with the routine use of anticoagulants (Heparin is the most common)
Anticoagulants also come with their own risk of side effects and complications

ACUTE RENAL SUPPORT
Hemodialysis
All variants of hemodialysis share the need for the following:
• vascular access – this carries the incurrent risks of complications such as infection or thrombosis
• extracorporeal circuit with artificial kidney – activation of complement and circulating neutrophils can lead to cardiorespiratory problems during dialysis, although this is more of a problem with cuprophane membranes than with the newer, more biocompatible membranes (eg, polysulphone and polyamide)
• anticoagulation – heparin is usually used, although prostacyclin can be used in the presence of a coagulopathy.

ACUTE RENAL SUPPORT
Hemodialysis
Potential problems include the following:
• dysequilibrium syndrome – rapid changes in plasma osmolality, leading to cerebral edema, and in some cases intracranial hypertension
• hypovolemia and hypotension
• fluid overload
• hypoxemia – possibly a result of inflammatory reactions initiated within the pulmonary microvasculature
• bleeding and vascular access complications.

PERITONEAL DIALYSIS

WHAT IS PERITONEAL DIALYSIS (PD)?
Peritoneal dialysis works by using the body's peritoneal membrane, which is inside the abdomen, as a semi-permeable membrane.
A specially formulated dialysis fluid is instilled around the membrane, using an indwelling catheter, then dialysis can occur, by diffusion
Excess fluid can also be removed by osmosis, by altering the concentration of glucose in the fluid.
Dialysis fluid is instilled via a peritoneal dialysis catheter, which is placed in the patient's abdomen, running from the peritoneum out to the surface, near the navel
Peritoneal dialysis is typically done in the patient's home and workplace, but can be done almost anywhere

ADVANTAGES OF PD
Can be done at home
Relatively easy for the client to learn
Easy to travel with, bags of solution are easy to take on holiday
Fluid balance is usually easier when the client is on PD than if the client is on HD

DIURETIC PHASE
Diuretic phase: The kidneys try to heal and urine output increases, but tubule scarring and damage occur.
Gradual decline in blood urea nitrogen and serum creatinine leveles, but still elevated
Continued low creatinine clearance with improving glomerular filtration rate
Hypokalemia
Hyponatremia
Hypovolemia

RECOVERY PHASE (CONVALESCENT)
Tubular edema resolves and renal function improves.
Increased glomerular filtration rate
Stabilization or continual decline in blood urea nitrogen and serum creatinine levels toward normal
Complete recovery (may take 1 to 2 years)